AB0348 DEPRESSION IN RHEUMATOID ARTHRITIS: PREVALENCE AND PHENOTYPIC CHARACTERISTICS - A SINGLE CENTER EXPERIENCE
Authors: C. E. Ionescu, C. Popescu, M. Agache, G. Dinache, C. Codreanu
Journal: Annals of the Rheumatic Diseases (2023)

<h3>Background</h3> Psychiatric comorbidities are frequent extra-articular manifestations in rheumatoid arthritis (RA) and depression is the most common [1]. A 2013 study estimated that 16.8 % of RA patients suffer from major depressive disorder, being more prevalent than diabetes, Parkinson's disease or cancer [2-3]. Patients with RA have constitutional symptoms, frequently encountered in depression, like fatigue, weight loss, insomnia and lack of appetite. The overlap of depression in inflammatory immune mediated diseases is recognized for some time [4]. Studies show that immune mediated inflammation affects and modulates neurogenesis, neurotransmission, neuroendocrine activity and neuroplasticity [5]. Depression has important effects on RA patients: worse prognosis, pain, fatigue, functional deficit, more comorbidities, higher rate of mortality, increased healthcare resource utilization and lowered quality of life [6]. <h3>Objectives</h3> The scope of this article is to highlight the importance of managing depression in RA. The primary objective was to estimate the prevalence of depression in a cohort of RA patients. The secondary objective was to describe the phenotypic characteristics of RA patients with depression. <h3>Methods</h3> RA patients from the Center of Rheumatic Diseases in Bucharest were included in the study if they were at least 18 years-old and if they had two or three follow-ups, after 2019. The protocol included collection of demographical, clinical and biological data. Prevalence of depression is derived from patients' medical history, known depression. Demographical characteristics and RA phenotype were compared between the two groups. Disease activity was estimated with DAS28 and its components, tender joint count, swollen joint count, CRP and were followed over time to compare disease activity between patients with known depression and patients without depression. <h3>Results</h3> We collected data from 203 patients with RA, among whom 37 were known with depression, generating a prevalence of 18.2%. A meta-analysis from 2013 reported that 16.8 % patients with RA suffer from a major depression disorder [1]. Most of the patients with depression were women (87.2%). Female sex is a potential risk factor for depression [7]. The prevalence of active smoking among the depression subgroup was higher (8.1%, 1.8%, p = 0.041). Depression is a known risk factor for negative behaviors like smoking [8]. Patients had a longer disease duration (in median, 13 years compared to 10 years, p = 0.059) and also the seropositivity prevalence was lower. In 2022 a correlation between depression and seronegative RA was found [9]. DAS28 and the components of DAS28 were higher in the depression RA subgroup; DAS28 was higher at all time points (p &lt; 0.001). Higher tender joint count was expected (p &lt; 0.001), but swollen joint count was also higher among depressive RA patients (p &lt; 0.001), as well as CRP (p = 0.009, Figure 1). <h3>Conclusion</h3> Depression is prevalent among RA patients and it has an important impact on the quality of life; so depressive symptoms should be addressed in clinical practice. The correlation between the prognosis of rheumatic disease and depression is strong, regardless of the direction of causality. The assessment of depression could be a psychomarker for assessing RA prognosis. DAS28 is used to make therapeutic decisions, so given that depression scores increase DAS28, it follows that they also influence therapeutic decisions. <h3>References</h3> [1] Morf H et al. <i>Clin Rheumatol</i> 2021, 40(5):1779-1787. [2] Overman CL et al. <i>Arthritis Care Res (Hoboken</i>) 2014, 66(5):671-678. [3] Jamshidi T et al. <i>Open Access Rheumatol</i> 2019, 11:53-59. [4] Nerurkar L et al. <i>Lancet Psychiatry</i> 2019, 6(2):164-173. [5] Muller N et al. <i>Mol Psychiatry</i> 2007, 12(11):988-1000. [6] Yilmaz V et al. <i>Eur J Rheumatol</i> 2017, 4(2):127-132. [7] Kim SY et al. <i>Rheumatology (Oxford</i>) 2020 Aug 1;59(8):1889-1897. [8] Englbrecht M et al. <i>PLoS One</i> 2019, 14(5):e0217412. [9] Kwiatkowska B et al. <i>Reumatologia</i> 2018, 56(4):219-227. <h3>Acknowledgements:</h3> NIL. <h3>Disclosure of Interests</h3> None Declared.